Obesity Accelerates Age Defects in Mouse and Human B Cells
Daniela Frasca1,2, Bonnie B Blomberg1,2
1Department of Microbiology and Immunology, University of Miami Miller School of Medicine, Miami, FL, United States.
Frontiers in Immunology
|September 28, 2020
Summary
Obesity drives chronic inflammation, termed inflammaging, increasing disease risk. Weight reduction can improve immunity and lower the risk of chronic diseases in obese and older individuals.
Area of Science:
- Immunology
- Gerontology
- Metabolic Syndrome
Background:
- Obesity is linked to chronic low-grade systemic inflammation (inflammaging), mirroring aging.
- This inflammation elevates the risk of age-related chronic diseases.
Purpose of the Study:
- To review the impact of obesity on immune cell function and inflammation.
- To explore the role of leptin in obesity-induced immune dysregulation and accelerated aging.
Main Methods:
- Review of existing literature on obesity, inflammation, and immune responses.
- Analysis of molecular mechanisms, including the role of adipokines like leptin.
Main Results:
- Obese adipose tissue recruits immune cells, releasing pro-inflammatory mediators.
- Leptin contributes to reduced protective antibody generation and increased autoimmune antibodies.
- Obesity accelerates immune defects, including B cell immunosenescence.
Conclusions:
- Obesity exacerbates inflammaging and immune system aging.
- Weight reduction programs are crucial for improving immunity and mitigating chronic disease risk.
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